Inhibitory Effect of Apolipoprotein A-I on Eosinophils in Allergic Rhinitis in vitro and in vivo

IF 3.7 3区医学 Q2 ALLERGY Journal of Asthma and Allergy Pub Date : 2024-02-13 DOI:10.2147/jaa.s449948

Yinhui Zeng, Jinyuan Li, Yueqiang Wen, Haiqing Xiao, Chao Yang, Qingxiang Zeng, Wenlong Liu

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Abstract

Purpose: Eosinophils have pivotal roles in the development of allergic rhinitis (AR) through the release of cytotoxic substances. Apolipoprotein A-I (Apo-AI) exhibits a strong inhibitory effect on eosinophil infiltration in allergic diseases. Nevertheless, the precise impact of Apolipoprotein A-I on eosinophils remains uncertain.
Methods: Our study recruited a total of 15 AR children and 15 controls. The correlation between Apo-AI expression and the counts of blood eosinophils was examined. Flow cytometry was employed to assess the role of Apo-AI in eosinophil apoptosis and adhesion. The Transwell system was performed to conduct the migration assay. An animal model using AR mice was established to test the effect of Apo-AI on eosinophils.
Results: Serum Apo-AI were negatively related to eosinophils counts and eosinophil chemotactic protein levels in AR. Apo-AI exerts a pro-apoptotic effect while also impeding the processes of adhesion, migration, and activation of eosinophils. The apoptosis triggered by Apo-AI was facilitated through the phosphoinositide 3-kinase (PI3K) pathway. The chemotaxis and activation of eosinophils, which are influenced by Apolipoprotein A-I, are regulated through the PI3K and MAPK signaling pathways. Apo-AI treated mice presented with decreased blood and nasal eosinophilic inflammation as well as down-regulated eosinophil related cytokines.
Conclusion: Our findings provide confirmation that Apo-AI exhibits inhibitory effects on the function of eosinophils in allergic rhinitis. This suggests that Apo-AI holds potential as a therapeutic target for future treatment strategies.

Keywords: apolipoprotein A-I, eosinophils, allergic rhinitis, apoptosis, adhesion, migration, activation

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载脂蛋白 A-I 对过敏性鼻炎嗜酸性粒细胞的体外和体内抑制作用

目的：嗜酸性粒细胞通过释放细胞毒性物质在过敏性鼻炎（AR）的发病过程中起着关键作用。载脂蛋白 A-I（Apo-AI）对过敏性疾病中嗜酸性粒细胞的浸润有很强的抑制作用。然而，载脂蛋白 A-I 对嗜酸性粒细胞的确切影响仍不确定：我们的研究共招募了 15 名 AR 儿童和 15 名对照组儿童。方法：我们的研究共招募了 15 名 AR 儿童和 15 名对照组儿童，研究了载脂蛋白 A-I 表达与血液中嗜酸性粒细胞数量之间的相关性。采用流式细胞术评估载脂蛋白 AI 在嗜酸性粒细胞凋亡和粘附中的作用。采用 Transwell 系统进行迁移试验。利用 AR 小鼠建立动物模型，测试载脂蛋白 AI 对嗜酸性粒细胞的影响：结果：血清载脂蛋白 AI 与 AR 小鼠的嗜酸性粒细胞数量和嗜酸性粒细胞趋化蛋白水平呈负相关。载脂蛋白 AI 具有促进嗜酸性粒细胞凋亡的作用，同时还能阻碍嗜酸性粒细胞的粘附、迁移和活化过程。载脂蛋白 AI 引发的细胞凋亡是通过磷酸肌酸 3- 激酶（PI3K）途径促进的。受载脂蛋白 A-I 影响的嗜酸性粒细胞的趋化和活化是通过 PI3K 和 MAPK 信号通路调节的。载脂蛋白 A-I 治疗小鼠的血液和鼻腔嗜酸性粒细胞炎症减少，嗜酸性粒细胞相关细胞因子下调：我们的研究结果证实，载脂蛋白 AI 对过敏性鼻炎中嗜酸性粒细胞的功能具有抑制作用。关键词：载脂蛋白 A-I；嗜酸性粒细胞；过敏性鼻炎；凋亡；粘附；迁移；活化

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来源期刊

Journal of Asthma and Allergy Medicine-Immunology and Allergy

CiteScore

5.30

自引率

6.20%

发文量

185

审稿时长

16 weeks

期刊介绍： An international, peer-reviewed journal publishing original research, reports, editorials and commentaries on the following topics: Asthma; Pulmonary physiology; Asthma related clinical health; Clinical immunology and the immunological basis of disease; Pharmacological interventions and new therapies. Although the main focus of the journal will be to publish research and clinical results in humans, preclinical, animal and in vitro studies will be published where they shed light on disease processes and potential new therapies.